Intake of water with high levels of dissolved hydrogen (H2) suppresses ischemia-induced cardio-renal injury in Dahl salt-sensitive rats
Background. Hydrogen (H2) reportedly produces an antioxidative effect by quenching cytotoxic oxygen radicals. We studied the biological effects of water with dissolved H2 on ischemia-induced cardio-renal injury in a rat model of chronic kidney disease (CKD). Methods. Dahl salt-sensitive rats (7 week...
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Veröffentlicht in: | Nephrology, dialysis, transplantation dialysis, transplantation, 2011-07, Vol.26 (7), p.2112-2118 |
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Zusammenfassung: | Background. Hydrogen (H2) reportedly produces an antioxidative effect by quenching cytotoxic oxygen radicals. We studied the biological effects of water with dissolved H2 on ischemia-induced cardio-renal injury in a rat model of chronic kidney disease (CKD).
Methods. Dahl salt-sensitive rats (7 weeks old) were allowed ad libitum drinking of filtered water (FW: dissolved H2, 0.00 ± 0.00 mg/L) or water with dissolved H2 produced by electrolysis (EW: dissolved H2, 0.35 ± 0.03 mg/L) for up to 6 weeks on a 0.5% salt diet. The rats then underwent ischemic reperfusion (I/R) of one kidney and were killed a week later for investigation of the contralateral kidney and the heart.
Results. In the rats given FW, unilateral kidney I/R induced significant increases in plasma monocyte chemoattractant protein-1, methylglyoxal and blood urea nitrogen. Histologically, significant increases were found in glomerular adhesion, cardiac fibrosis, number of ED-1 (CD68)-positive cells and nitrotyrosine staining in the contralateral kidney and the heart. In rats given EW, those findings were significantly ameliorated and there were significant histological differences between rats given FW and those given EW.
Conclusion. Consumption of EW by ad libitum drinking has the potential to ameliorate ischemia-induced cardio-renal injury in CKD model rats. This indicates a novel strategy of applying H2 produced by water electrolysis technology for the prevention of CKD cardio-renal syndrome. |
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ISSN: | 0931-0509 1460-2385 |
DOI: | 10.1093/ndt/gfq727 |